Cardiac Lecture 2

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cmatthews
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220872
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Cardiac Lecture 2
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2013-05-23 19:21:25
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BC CRNA Cardiac Lecture
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Lecture 2 5/23/13
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  1. What does this say about the A. P. and muscle contraction?
    • muscle tension develops after the plateau of the action potential.
  2. What is Isovolumetric contraction?  (end of diastole)
    • At start of ventricular contraction
    • After closure of AV valves and before opening of aortic & pulmonic valves
    • Contraction of the ventricle but no emptying
  3. What is Isovolumetric relaxation? (end of systole)
    • At end of systole
    • After aortic & pulmonic valves close and before AV valves open
  4. Define End Diastolic Volume (EDV)
    Volume at the end of ventricular filling
  5. Define End Systolic Volume (ESV)
    Volume at the end of systole (after ejection)
  6. Define Stroke Volume (SV)
    • Volume of blood ejected during each contraction.
    • EDV-ESV = SV
  7. Define Ejection Fraction (EF)
    • Fraction of blood ejected during each contraction
    • SV/EDV = EF
  8. Define Preload
    • Cardiac filling pressure
    • End-diastolic pressure
    • Volume that fills ventricle prior to contraction. Reflects the amount of tension on the muscle when the ventricular muscle starts to contract.
    • Can be thought of as LVEDP or LVEDV. CVP or wedge pressure (LA)
  9. Define Afterload
    • Systemic arterial pressure
    • Determines the tension that must develop in ventricular muscle fibers
    • It’s the systolic pressure during the period of ejection. Usually think of afterload as resistance, but resistance is really in the form of pressure.
  10. What is cardiac work? Where does the energy come from to do this work?
    • Contraction (contractility)
    • Work requires energy, comes from the oxidation of fatty acids (mostly) as well as lactate and glucose. All the biochemistry pathways we looked at last semester.
  11. What is the Frank Starling Mechinism in relation to the heart?
    • With other factors equal, stroke volume increases with increased cardiac filling (end-diastolic volume)
  12. Besides the frank starling mechanism, what other factor helps increase pumping with increased volume?
    stretching of RA, that will increase the HR by 10-20%, we know HR x SV = CO, if we increase the HR we’ll also increase CO.
  13. TRUE or FALSE. At rest, the EDV is close to the optimal overlap of actin/myosin filaments.
    FALSE. At rest the EDV doesn’t come anywhere near the optimal overlap of actin/myosin, essentially mean we have a pretty good reserve capacity. We’re not working at maximum at rest
    • nIncreased venous return → ↑ ventricular filling → ↑ EDV
    • Stroke volume ↑s as ventricle contracts at higher preload with afterload held constant
  14. The heart uses energy to do work in 2 forms. What are they?
    • 1. Pressure/volume work (or external work). Used to move blood from low pressure veins to high pressure arteries.
    • 2. Kinetic energy of blood flow, accelerated flow
    • through the system or ejection through Ao or pulmonic valves.
  15. The diastolic pressure doesn’t really rise until resting ventricle contains about ____ of blood.
    150ml
  16. max systolic pressure is ___ of LV but in contrast the normal RV max systolic pressure is more like ___mmHg.
    • 250 of LV
    • 60-80 of RV
  17. Describe the phases of the external work (pressure/volume) loop.
    • Phase 1: period of ventricular filling. Starts at point of End systolic volume (around 50ml), at end of ejection, ventricular filling. 
    • Phase 2: The period of isovolumetric contraction. So the volume isn’t changing, pressure is building, 
    • Phase 3: period of ejection, initially pressure increases and then pressure and volume both go down.
    • Phase 4:  which is isovolumetric relaxation.
  18. Increased preload,(at constant aortic systolic & diastolic pressure and inotropy) will _____ SV and ________ESV. EF will _________
    increase SV and no change to ESV. EF increases slightly
  19. Decreased preload (↓EDV), (at constant aortic systolic and diastolic pressures and inotropy) will ____ the SV and _______the ESV. EF will _________
    decrease the SV (less for ventricle to eject) and the ESV remains unchanged. EF decreases slightly.
  20. In our practice, what do we usually do to treat hypoension during induction?
    So increasing preload is common intervention in our practice. Usually 1st step of tx hypotension in induction, we’ll increase the SV by giving fluid bolus. 
  21. So there is a certain stress within the wall of ventricle that’s necessary to generate a pressure to open an aortic valve, that stress is called ___________.
    AFTERLOAD
  22. For afterload talking about the pressure in the Aorta or arterial pressure as being somewhat equivalent to (approximation but not identical to) afterload. Why is this not exactly true?
    • Ohm’s law, CO= (MAP-CVP)/SVR.
    • Consider the patient that has HF, a dilated LV, and a low CO. If we give the patient a drug to decrease the SVR, a vasodilator or afterload reducer, the CO will increase, but we haven’t changed BP or MAP, so the aortic pressure (Systemic arterial pressure) is an approximation of afterload but more complex than that.
  23. The pt w/chronic HTN has increased afterload,
    What does this mean for the pressure in the ventricle?
    the pt must get higher ventricle pressure and therefore wall tension. To overcome the aortic pressure and open the valve to eject the stroke volume
  24. Increased afterload (increased aortic pressure), at a constand preload (EDV) and inotropy will _________ the SV and ESV will ______. The EF _________
    decreases the SV and ESV will increase. the EF decreases
  25. Decreased afterload (decreased aortic pressure), at a constant preload (EDV) and inotropy will _____ the SV and ESV will _________. EF will ______
    increase the SV and decrease the ESV. EF will increase.

  26. what does this picture represent regarding afterload and SV?
    Effects in changes in afterload on Frank starling's curve. Increased afterload moves A to B. and Decreased afterload moves A to C.
  27. When we increase afterload, which phase is longer?
    Phase 2. Represents a greater part of systole. Isovolumetric contraction, it needs to build up more pressure to be able to open Aortic valve, more times is spent in this. Systole is fixed amount of time, there is less time available for cardiac muscle fiber shortening and ejection, less time for that, and consequently, stroke volume will be less.
  28. Increased inotropy, at constant preload (EDV) & constant aortic systolic and diastolic pressures,  will ______ SV and ________ ESV. The EF will _______.
    Increase SV and decrease ESV. EF will increase.
  29. Decreased inotropy, at constant preload (EDV) & constant aortic systolic and diastolic pressures, will ________ SV and ______ESV. The EF will _______.
    decrease SV and increase ESV. The EF will decrease.
  30. The slope of the pressure volume curves represents end systolic volume pressure volume
    relationship (ESPVR). If we increase contractility or intropy we’ll __________ the slope of that relationship (the slope of that line)
    increase (the ventricle is able to generate more pressure at a given LV volume)

  31. what does this picture represent regarding inotropy and SV?
    • Increased contractility, or increased inotropy, the SV will increase going from A to C (if A is normal)
    • Decreased contractility we’d be going from A to B.
  32. What happens if we increase preload (EDV) at a constant inotropy? SV ______. ESV ________.
    • SV increases, ESV increases slightly because afterload (aortic pressure) increases.
    • (increased preload will increase SV and increase BP therefore increase afterload)
  33. What would happen if we decreased preload at a constant inotropy? SV_____. ESV _______.
    SV decreases. ESV decreases slightly because afterload (aortic pressure) decreases.
  34. What would happen if we increased afterload at constant intropy? SV ______. ESV _______. EDV ______.
    SV slightly decreases. ESV increases and EDV slghtly ncreases secondarily.
  35. What would happen if we decreased afterload at a constant inotropy? SV____. ESV _____. EDV ____.
    SV slightly increases. ESV decreases and EDV slightly decreases secondarily.
  36. What happens if we increase intropy? SV _____. ESV _______. EDV _______. EF ______.
    SV increases. ESV decreases and EDV decreases secondarily (small amt). EF increases
  37. What happens if we decrease inotropy. SV____. ESV_____. EDV _______. EF________.
    SV decreases. ESV increases.  EDV increases secondarily a small amount. EF decreases.
  38. What happens to the heart if there is a high amount of K+ in the ECF?
    the heart becomes dilated and flaccid, the HR will slow, conduction through the AV bundle will be blocked. The resting membrane potential inside the cell (is more negative) the cell is hyperpolarized, too many positive ions outside, so the membrane is hyperpolarized so cardiac conduction isn’t strong.
  39. What happens to the heart if Ca+ is too low?
    decreased cardiac contractility
  40. What happens to the heart if the Ca+ is too high?
    heart becomes spastic d/t excess Ca+ ions
  41. How does temperature effect CO?
    actual effect on contractility depends on the duration of hyperthermia. Exercise, body temp increases, contractility increase, but if prolonged hyperthermia, that accelerated metabolism will deplete metabolic stores and a decrease in contractility will result.
  42. What affect does aortic (Arterial) pressure have on cardiac output?
    won’t decrease CO, until it reaches about  160mmHg. With normal systolic pressures, not really a problem, more determined by venous return.
  43. SNS can increase the HR to _____
    200 or more
  44. SNS can ______the force of the contraction
    increase
  45. By stimulating the SNS, we can get _______x increase in CO between an increase in contractility and an increase in HR.
    2-3x
  46. Inhibiting the SNS will decrease both HR and pumping by around _____%.
    30%
  47. Why does the PNS have a bigger effect on HR than on contractility?
    most of those vagal fibers  go to the atria, so there is abigger effect on HR then on the strength of the contraction
  48. Vagal stimulation can cause a decrease in pumping by _______%.
    50% or more
  49. Profound vagal stimulation can cause_________
    asystole (although usually a ventricular escape of about 30)
  50. Tell me about S1 sound
    • Closure of AV valves at start of systole
    • Duration of 0.15 sec
    • Soft
  51. Tell me about S2 sound
    • Closure of semilunar valves immediately after the end of systole
    • Duration of 0.12 sec
    • Loud & sharp when aortic or pulmonary artery pressure is high
    • May hear physiologic “split”
  52. Tell me about S3 sound
    • Rapid inflow of blood into ventricle
    • 1/3 of the way through diastole
  53. Tell me about S4 sound
    • Immediately before S-1 if high atrial pressure or stiff ventricle in ventricular hypertrophy
    • Due to ventricular filling
  54. What is the basic route of conduction through the heart
    • SA node
    •   ↓
    • Internodal pathways
    •   ↓
    • AV node
    •   ↓
    • AV bundle
    •   ↓
    • L & R Bundle branches
  55. What is the small flat strip of specialized cardiac muscle in posterior wall of lateral RA. Just below and lateral to entrance of SVC.
    SA node
  56. Does the SA node have contractile fibers?
    No. The SA node itself doesn’t have contractile fibers, connects directly to Atrial fibers, will carry AP immediately to atrial muscle.
  57. Tell me what's different about the pacemaker AP compared to the rest of the cardiac AP
    • Its slower to develop and the morphology is different. There is a slower initial depolarization phase, (phase 4) there is slower phase 0, essential no over shoot and no plateau. And then finally a slower repolarization process too.
    • Considered an unstable resting membrane potential in these pacer cells.
  58. Pacer cells resting membrane potential is ___mV
    -55mV (other cardiac cells it's more like -90mV) This is because the cell membranes are leaky to Na & Ca ions, those are mostly in ECF (if they leak they are leaking inside, bringing positive charges, bringing inside potential to more positive (less negative) how we get -55mV. *Fast Na channels, the inactivation gate (inner gate) is closed at -55mV & when the potential is around the -55mV, it stays closed. So consequently the fast Na channels don't start the A. P. It has to be the slow Ca channels, that can become activated, and open to cause AP, because of that the AP looks slow
  59. What are the factors responsible for self excitation?
    • High ECF sodium
    • Open sodium channels
    • Sodium leaks → inside
    • Resting potential ↑s
    • At -40 mV sodium-calcium channels become
    • “activated” → action potential
  60. Two things happen to prevent a permanent depolarization of SA node fibers. What are they?
    • . The first thing is the Na/Ca channel (slow channels) become inactivated and close after opening. And then K+ channels open. So influx of Na and Ca will stop because the Na & Ca channels close and w/K opening, K will exit the cell  to restore the resting membrane potential. 
    • The potential will just to -55mV or so, and then Na/Ca leakage again starts, the threshold drifts up to now -40 that action potential will start again and the process repeats itself.
  61. What is  in the posterior wall of the RA, just behind the TV?
    The AV node
  62. The SA node is connected to the AV node through  internodal pathways. What is the approximate time interval between the start of the impulse in the SA node to arrival to Av node
    0.03sec
  63. How long is the delay in the AV node before the AP goes to AV bundle and into the ventricles.
    0.09 sec
  64. How do we get slower conduction through the AV node?
    The slower conduction is due the fact there are fewer gap junctions so there is resistance to conduction of those ions.
  65. Why do we like the conduction delay between the atria and ventricles?
    permits atria to empty and ventricles to fill prior to contraction
  66. Describe the purkinje system
    • Large fibers
    • Transmit action potential 6 times greater than in ventricle and 150 times greater than AV node
    • Highly permeable gap junctions at intercalated discs (ions flow easily)
    • Few myofibrils
    • Forward conduction only
  67. How does the impulse spread once in the ventricles?
    The impulse will spread across both ventricles from endocardial to epicardial and spirals.
  68. How does PNS affect the transmission of the A.P to the AV node?
    vagal stimulation will slow, decrease transmission on to AV node and to ventricles, decrease pumping
  69. How does PNS hyperpolarize a cell?
    NT at end organ is Ach when it’s released it will increase permeability of muscle fiber to K+, because K+ is more inside cell it leaks to outside the cell. The cell becomes hyperpoloarized, it takes longer to get to threshold, that slows the rate of autmaticity. Same effect can occur on AV node as well, decrease excitation on those fibers as well.
  70. How does the SNS affect self excitation of the pacer cells?
    NT at the end organ is Norepi, it will increase permeability of the fiber to Na and Ca ions, they’ll move in and cause the resting membrane potential to be more positive, closer to  threshold, accelerating the self excitation and increasing the HR.
  71. P wave on the EKG represents
    atrial depolarization (occurs immediately before atrial contraction)
  72. QRS on the EKG represents
    ventricular depolarization
  73. T wave on the EKG represents
    Ventricular repolarization
  74. V1 and V2 are predominately negative or positive?
    negative
  75. V4, V5, V6 are more positive or negative?
    positive
  76. V3 is more positive or negative?
    Tricky! It's transitional

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